Myocardial contractile function is impaired when ventricular hypertrophy and congestive heart failure result from a pressure overload on the heart. Little is known of the potential for recovery of function or of the basic physiological mechanisms which underly these conditions. Until these basic mechanism are understood there is little potential of enhancing the capability for recovery or of opening new avenues for therapeutic intervention. This proposal has the goal of utilizing animal models of ventricular hypertrophy and congestive heart failure for obtaining an understanding of basic mechanisms which may be implicated. It is proposed to combine: hemodynamic analysis by cardiac catheterization of the whole animal; myothermic analysis of the isolated heart by calorimetry; and in vitro muscle biochemistry of myosin-adenosine tri phosphotase activity to elucidate basic mechanism which may be implicated in the myocardial defect which results from pressure overload hypertrophy and congestive heart failure. Particular objectives include elucidation of: 1) Myocardial calcium activation energetics; 2) Myocardial force and pressure development energetics; 3) Metabolic substrate utilization in oxidative phosphorylation; and 4) Myosin ATPase activity and kinetic reaction velocity. It is submitted that investigaton of these parameters in an animal model of reversible ventricular hypertrophy will provide a valid first step in the progression of knowledge that will lead from mammalian papillary muscle data to a state where positive applications with relevance to man may be envisioned.